Beyond The Basics: Four Fatal Pulmonary Problems

OBJECTIVES

• Review pathophysiology of four pulmonary problems
• Discuss prehospital management of these patient groups

     This article reviews four different pulmonary problems, the pathophysiology behind them and current treatment. The problems were chosen for their frequency and criticality, and to provide insight into assessment, diagnosis and treatment.

ASPIRATION

     Patients with an altered mental status are at high risk for aspiration. We see patients on the street who are experiencing conditions ranging from stroke to overdose to codes that include this risk.

PATHOPHYSIOLOGY INSIGHTS

     Aspiration can cause two potentially fatal conditions, especially in patients who are in a weakened condition. Aspiration pneumonia, usually a bacterial infection from organisms commonly found in the upper airway, occurs when oropharyngeal contents pass into the tracheobronchial tree.

     While pneumonia is a serious infection, it has a relatively low mortality. The condition that caused aspiration, combined with the increased potential for sepsis, raises the risk of serious complication or death. This condition is less serious, with a mortality rate between 1%—25%, depending on the patient's co-exisiting conditions and whether bacteremia is present.

     Another term that is sometimes used synonymously with aspiration pneumonia is aspiration pneumonitis. The terms are not synonymous, however. Aspiration pneumonitis is a much more serious condition, with a mortality of up to 70%.

     Aspiration pneumonitis involves aspiration of stomach contents into the tracheobronchial tree. These substances have a pH of about 2.5 (a very strong acid), which causes physical damage to airway structures.

SIGNS AND SYMPTOMS (IMMEDIATELY POST-ASPIRATION)

• Altered mental status
• Evidence of recent vomiting
• Abnormal respiratory sounds (including rhonchi, gurgling, wheezing and diminished sounds).

TREATMENT

     Patients seen in the field are suffering from the more acute effects of aspiration rather than the chronic infection seen later in the hospital, although airway obstruction or reactivity (constriction) may occur in response to the aspirated materials. Serious systemic complications begin anytime from an hour to days after aspiration.

     Patients who have aspirated should receive immediate orotracheal suctioning. If necessary, BLS care should include ventilations delivered in a slow, consistent fashion. Excessive pressure will close the glottic opening, diverting delivered ventilations to the esophagus and stomach and resulting in vomiting.

     There are many false preconceptions about suctioning theory and procedure. Since some of our procedures have been developed from hospital theory, they may not fully apply to the field setting. One of these is the concept of suctioning for no longer than 15 seconds. While this may apply to intubated patients in a controlled setting, the dilemma in the field begins on the 16th second of vomiting, and often continues longer. The more correct rule is: Suction completely and as quickly and efficiently as possible by rolling the patient to his side and using a large-bore catheter or tubing to remove vomit. Perform finger sweeps with a gloved hand when safe to do so.

     Since aspiration of significant quantities of acid is most frequently fatal, suction may be required for longer periods. Essentially, we are balancing the potential risk of death from aspiration pneumonitis against the risk of death from hypoxia.

     Another preconception is the ability to preoxygenate before suctioning in many cases. Unless you are able to predict vomiting several minutes before it occurs, the more correct rule would be to provide consistent, quality ventilations with supplemental oxygen so that any breaks will leave the patient oxygenated to the fullest extent possible. Never ventilate immediately after the patient vomits or in the presence of secretions.

     Advanced life support providers will intubate patients to provide optimal airway control. Preoxygenation may be performed prior to providing orotracheal suctioning.

ASTHMA

     Asthma is a common presentation in EMS. While the ability to administer nebulized medications or assisted metered dose inhalers provides some of the most dramatic improvements seen in the field, those providers who have found patients in a severe attack not reversible by inhaled medications truly know why asthma is listed in this article as a fatal condition.

     While deaths from asthma have decreased since the early 1990s, knowing the etiologies and pathophysiology of asthma will improve understanding and care of this common complaint.

PATHOPHYSIOLOGY INSIGHTS

     Asthma is a reactive airway disease. It is an episodic condition that results in sudden constriction of the smooth muscle in the bronchi and bronchioles. A secondary result of asthma—and one which causes the longer-term effects and serious consequences of the disease—is inflammation of the airways and the production of mucus.

     A classic presentation of severe asthma results when a patient takes a metered dose inhaler or nebulizer at home to deal with dyspnea—the urgent presenting symptom. These medications relieve smooth muscle contraction through their beta2 agonist effects. Without medications to deal with airway inflammation and mucus production, subsequent attacks will follow, as airway resistance remains high from the persistent inflammatory processes.

     This is why clinicians consider overuse of inhaled beta agonists a sign of uncontrolled asthma and a predictor of serious attack. Generally, a patient shouldn't need to use a rescue inhaler more than two or three times per week. More frequent use indicates the need for inhaled corticosteroids or other medications to deal with long-term reactivity and inflammation.

     Asthma has several factors that are considered "triggers," including viral respiratory infection; exposure to allergens, smoke or inhaled chemicals; exercise; aspirin use; and weather changes—especially cold, dry weather. Identifying these will be helpful as part of your patient history and differential diagnosis.

SIGNS AND SYMPTOMS

     The classic sign of asthma is wheezing; however, relying on wheezing as the singular sign of asthma limits a clinician from finding other valid signs and symptoms to be used in the diagnostic process.

     Simply stated, the patient may not wheeze when bronchioles are too narrowed and inflamed to pass significant quantities of air and produce wheezing any longer—a grave sign. In some patients, especially children, cough is the primary presenting sign of bronchoconstriction.

     When listening to lung sounds and observing respirations, the inspiration to exhalation ratio is also important. The asthma patient will take a breath in with relative ease. Exhalation will be more difficult and prolonged. An increased expiratory phase is an overlooked but important sign of asthma. In severe cases, exhalation may take up to three times longer than inspiration. This can be seen in capnography as the classic "shark fin" pattern. Peak flow measurement is also increasingly common in EMS systems.

     While some patients who appear to have asthma do in fact have it, other conditions may mimic asthma. The classic "cardiac asthma" refers to the wheezing that can be present in congestive heart failure. Chronic obstructive pulmonary conditions (emphysema, chronic bronchitis) are other key differential diagnostic considerations.

SIGNS AND SYMPTOMS

• Dyspnea
• Wheezing
• Coughing
• Tripod position
• Accessory muscle use
• Reduced ability to speak.

TREATMENT

     Beta₂ agonists are the mainstay of treatment. These may be delivered by metered dose inhaler or nebulizer. While ALS providers—and an increasing number of BLS providers—are now administering nebulized medications, a properly delivered inhaler using a spacer device has been shown to provide significant bronchodilation.

     A benefit of nebulized medications is the ability to deliver them continuously. Many protocols are moving toward repeated or continuous nebulized medication, which may also be beneficial during prolonged transport times.

     Since bronchial smooth muscle tone is regulated by both adrenergic and cholinergic receptors, medications such as ipratropium (found commonly in Combivent inhalers) and Duoneb for nebulization are used in severe asthma attacks.

     Patients who are experiencing a severe attack and are not responsive to inhaled treatments may require subcutaneous administration of epinephrine or terbutaline. Inhaled bronchodilators must be topically deposited at the site of bronchoconstriction to be effective. In cases of maximal constriction, where air movement in the distal bronchioles is severely diminished or absent, the medication is unable to be delivered and topically deposited. Therefore, the efficacy of the medication would be very limited at best. Extreme caution must be used with epinephrine administration due to cardiac side effects. The patient can become hypoxic and hypercarbic from the existing asthma attack, which is likely to lead to acidosis. Stimulation of the beta₁ receptors will increase the myocardial workload and myocardial oxygen demand in an already hypoxic environment and may lead to cardiac dysrhythmias or myocardial infarction. Magnesium sulfate may be administered via slow IV (e.g. 2g over 20 minutes) in situations where bronchoconstriction is resistant to other treatments.

CONGESTIVE HEART FAILURE

     Congestive heart failure is another common EMS response with varied patient presentation. While patients with CHF have a high incidence of hospital admissions and death, the subjective feeling of those patients is that they are unable to breathe and frequently believe they are about to die.

PATHOPHYSIOLOGY INSIGHTS

     Simply stated, congestive heart failure is inability of the pump to maintain circulation of blood. The pump failure may occur because of damage (myocardial infarction) or weakening (e.g., hypertrophy) of the left ventricle, which causes increased hydrostatic pressure in the pulmonary capillaries. The increased hydrostatic pressure will push fluid out of the capillary and into the interstitial space surrounding the alveoli and distal bronchioles. The additional fluid increases the alveolar/capillary interface, the space between the alveoli and capillaries, making gas exchange less effective. A reduction in the effectiveness of oxygen transfer from the alveoli to the capillary and carbon dioxide from the capillary to the alveoli will occur. As the condition progresses, fluid moves into the alveoli, worsening the gas exchange and resulting in worsening hypoxia.

     Overlooked in physical examination findings is the progressive nature of this condition. Patients tend to call EMS when the condition suddenly worsens—maybe in the middle of the night, where they present with severe dyspnea and anxiety, and are found in a tripod position with feet dangling from the bed or chair. Interestingly, the patient will dangle his feet to allow gravity to pool blood in the lower extremities and reduce the venous return in an attempt to decrease hydrostatic pressure inside the pulmonary capillaries.

     While the patient in this scenario will generally say he suddenly couldn't breathe, especially at night while supine (paroxysmal nocturnal dyspnea), a careful history usually reveals that he had some combination of dyspnea on exertion, orthopnea, weight gain or noticeable peripheral edema for days to weeks prior to this call (unless a sudden MI caused the condition).

     This should cause prehospital clinicians to look for these symptoms in the history and physical examination of any patient with a cardiac or respiratory complaint, as well as in patients who have risk factors for cardiac conditions in presentations of weakness, anxiety or malaise, in order to identify heart failure before a critical stage.

SIGNS AND SYMPTOMS

• Dyspnea may be experienced during activity (dyspnea on exertion), at rest or as paroxysmal nocturnal dyspnea
• Tachycardia and tachypnea
• Jugular venous distention (late and more indicative of right-side heart failure)
• Lung sounds including wheezes and rales
• Severe anxiety (secondary to hypoxia)
• Peripheral edema and weight gain.

TREATMENT

• Oxygen based on level of distress and hypoxia
• Position of comfort (usually sitting) unless resuscitation or ventilation is required
• Nitrates (SL nitroglycerin if systolic pressure greater than 90mmHg)
• Diuretics (furosemide 40—80mg slow IV)
• Continuous positive airway pressure (CPAP).

PULMONARY EMBOLUS

     Pulmonary embolus is likely the most frequently fatal condition mentioned here, as well as the most difficult to diagnose. A significant number of pulmonary emboli are diagnosed at autopsy. It is believed that many sudden deaths are actually massive PE, as opposed to a cardiac incident.

PATHOPHYSIOLOGY INSIGHTS

     The majority of pulmonary emboli arise from deep vein thrombosis in a lower extremity. Occasionally emboli will form in upper extremities, as well as around heart valves and indwelling catheters.

     The size of the embolus will determine the severity of patient presentation, with larger emboli lodging in pulmonary artery bifurcations or in major branches. These larger emboli cause significant hemodynamic compromise and are frequently fatal. Smaller emboli travel distally in the pulmonary circulation and result in local signs and symptoms.

     It is not uncommon for a patient to experience multiple pulmonary emboli at the same time. Patients who have experienced prior emboli are at greater risk of emboli in the future.

     Since the size of the emboli can cause different effects, relating pathophysiology to signs and symptoms helps understand assessment findings. While larger emboli cause pronounced signs and symptoms, including altered mental status, severe hypoxia and hemodynamic compromise, smaller emboli can cause specific conditions in the lungs, such as pleuritic chest pain from an inflammatory response. Smaller emboli are more likely to cause these conditions in the lower lung lobes.

SIGNS AND SYMPTOMS

     While the size of pulmonary emboli will determine the signs and symptoms, it is important to note that patient presentations are extremely varied. It is a diagnosis that can be missed—even in the hospital. Diagnosis relies on a combination of suspicion based on presentation and history and in-hospital diagnostic testing.

     Signs and symptoms can include:

• Chest pain, which may be pleuritic
• Cough that may be productive with hemoptysis
• Wheezing
• Altered mental status and syncope
• Signs of shock, including diaphoresis, tachycardia, tachypnea and hypotension
• History or suspicion of deep vein thrombosis from factors including immobilization, surgery, trauma or pregnancy
• Localized rales or wheezes and alteration in heart sounds that are possible but difficult to obtain in the field.
• History of prior or suspected pulmonary emboli.

TREATMENT

• Oxygen based on level of hypoxia and respiratory distress
• Airway, breathing and circulatory support based on patient presentation and severity
• Transportation in a position of comfort.

CONCLUSION

     Prehospital clinicians at any level should remember that a thorough history followed by accurate assessment in any medical patient is the key to decision-making in differential diagnosis and care.

     Using this review of the basics with practical pathophysiology will help the prehospital provider at any level manage respiratory complaints.

     Daniel D. Limmer, AS, EMT-P, is a paramedic with Kennebunk Fire-Rescue in Kennebunk, ME.

     Joseph J. Mistovich, MEd, NREMT-P, is a professor and chair of the Department of Health Professions at Youngstown (OH) State University.

     William S. Krost, MBA, NREMT-P, is director of Emergency Services & Health System Access for Blanchard Valley Health System in Findlay, OH.